In this project we aim to provide a complete neural circuit diagram for certain elements of female reproductive behavior, and to analyze how estrogenic hormones affect the operation of the circuit so as to produce behavioral changes. I. Building on past work, we will finish describing, in quantitative physical terms, the cutaneous stimuli which trigger lordosis behavior in female rats. Then, using this stimulus information as a "key", we will use electrophysiological recording to "follow" the behavior-determining sensory information into and through the central nervous system. Recording from the first way station, the dorsal root ganglion, will be followed by recording from the dorsal horn of the spinal cord, and then from spinoreticular neurons, and then from reticular neurons in brainstem. II. Experiments on hormonal determinants of lordosis behavior in rats will be related to past work on estrogen binding by neurons. Quantitative studies on requirements for long-term estrogen action for lordosis will be done. Parallel effects of an anti-estrogen on estrogen-binding and reporductive behavior will be examined. Hormone uptake, lesion studies and implant results all indicate that ventromedial hypothalamic neurons are involved in lordosis control. We will study the axonal projections of these neurons, and will examine effects of ventromedial hypothalamic electrical stimulation on female reproductive behavior. III. Transection and lesion studies in the midbrain will be used to determine which hypothalamic outputs are crucial for lordosis. In turn, lower brainstem neurons carrying the hormone-dependent signal must be determined, and we know that the lateral vestibulospinal tract and medullary giant cell reticular formation are involved. These lower brain-stem cells will be characterized by electrophysiological techniques using acute and chronic single unit recording. The muscles which execute lordotic rump elevation have been determined. Electrophysiological experiments using this knowledge will be done to analyze spinal mechanisms and the final common pathway for the vertebral dorsiflexion of lordosis.